Please use this identifier to cite or link to this item: http://ir.swu.ac.th/jspui/handle/123456789/15222
Title: 5-HT2A receptor activation and nitric oxide synthesis: A possible mechanism determining migraine attacks
Authors: Srikiatkhachorn A.
Suwattanasophon C.
Ruangpattanatawee U.
Phansuwan-Pujito P.
Keywords: 1,2,5 dimethoxy 4 iodophenyl 2 aminopropane
biological marker
glyceryl trinitrate
nitric oxide
nitric oxide synthase
protein fos
serotonin 2A agonist
serotonin 2A receptor
sodium chloride
unclassified drug
nitric oxide
serotonin receptor
animal experiment
animal model
animal tissue
article
blood vessel innervation
brain blood flow
brain circulation
chronicity
controlled study
correlation analysis
disease course
Doppler flowmetry
drug exposure
evoked response
headache
hyperemia
immunohistochemistry
immunoreactivity
male
migraine
nerve fiber
neuromodulation
nociception
nociceptive receptor
nonhuman
pain assessment
priority journal
protein determination
protein expression
rat
regulatory mechanism
spinal cord dorsal horn
spinal nerve
synthesis
tail flick test
trigeminal nucleus
trigeminus ganglion
vasodilatation
animal
biosynthesis
human
metabolism
migraine
pathophysiology
physiology
randomization
Wistar rat
Animals
Cerebrovascular Circulation
Humans
Male
Migraine Disorders
Nitric Oxide
Nociceptors
Random Allocation
Rats
Rats, Wistar
Receptors, Serotonin
Issue Date: 2002
Abstract: Objective. To determine the effect of the 5-HT2A receptor in control of spinal nociception, cerebral circulation, and nitric oxide synthase (nNOS) expression in trigeminovascular neurons. Background. The plasticity of the 5-HT2A receptor is a possible factor determining the course of migraine. Up-regulation of this receptor has been demonstrated to correlate with the increasing frequency of migraine attacks and may underlie the development of chronic daily headache. Methods. Adult male Wistar rats were divided into groups receiving the 5-HT2A agonist, 1,2,5-dimethoxy-4-iodophenyl-2-aminopropane (DOI), nitroglycerin, or normal saline. The tail flick test and chemical nociception-evoked Fos-expression in dorsal horn neurons were used as indicators of nociception. Regional cerebral blood flow was monitored using laser Doppler flowmetry. Expression of Fos and nNOS was studied using immunohistochemical method. Results. Administration of DOI led to the shortening of tail flick latency (1.3 ± 0.2 and 7.2 ± 0.6 seconds for DOI-treated and control groups, respectively). The number of Fos-immunoreactive neurons was also greater in the DOI-treated group compared with the control group. DOI also produced long-lasting cerebral hyperemia (123% of baseline value) associated with the enlargement of perivascular nNOS-immunoreactive nerve fibers and increased nNOS-immunoreactive neurons in trigeminal ganglia and trigeminal nucleus caudalis. These findings resembled those observed in the rats exposed to nitroglycerin. Conclusion. Our results suggest that activation of the 5-HT2A receptor leads to an enhancement of NO production in trigeminovascular pathway. NO may trigger migraine attacks by inducing cerebral vasodilation and sensitizing the perivascular nociceptors and central nociceptive neurons in trigeminovascular system. Up-regulation of this pronociceptive receptor can increase headache attacks and contributes to the development of chronic daily headache.
URI: https://www.scopus.com/inward/record.uri?eid=2-s2.0-0036651874&doi=10.1046%2fj.1526-4610.2002.02142.x&partnerID=40&md5=01e218d06a5542e2b5a9f256d0419f3a
http://ir.swu.ac.th/jspui/handle/123456789/15222
ISSN: 178748
Appears in Collections:SCOPUS 1983-2021

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